Abstract
Signal transducer and activator of transcription 3 (STAT3) controls cell survival, growth, migration, and invasion. Here, we observed that STAT3 exerted anti-apoptotic effects in breast cancer cells. On the other hand, miR-17-5p induced apoptosis in breast cancer cells, and overexpression of miR-17-5p sensitized MCF-7 cells to paclitaxel-induced apoptosis via STAT3. Overexpression of STAT3 in MCF-7 cells decreased paclitaxel-induced apoptosis, but STAT3 knockout abolished the miR-17-5p-induced increases in apoptosis. Finally, miR-17-5p promoted apoptosis by increasing p53 expression, which was inhibited by STAT3. These results demonstrate a novel pathway via which miR-17-5p inhibits STAT3 and increases p53 expression to promote apoptosis in breast cancer cells.
Keywords:
STAT3; apoptosis; breast cancer; miR-17-5p; paclitaxel.
MeSH terms
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3' Untranslated Regions / genetics
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Antineoplastic Agents, Phytogenic / pharmacology
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Apoptosis / drug effects*
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Apoptosis / genetics
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Blotting, Western
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Breast Neoplasms / genetics
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Breast Neoplasms / metabolism
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Breast Neoplasms / pathology
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Cell Line, Tumor
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Cell Survival / drug effects
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Cell Survival / genetics
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Estrogen Antagonists / pharmacology
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Female
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Gene Expression Regulation, Neoplastic*
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Humans
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MCF-7 Cells
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MicroRNAs / genetics*
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Paclitaxel / pharmacology*
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Reverse Transcriptase Polymerase Chain Reaction
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STAT3 Transcription Factor / genetics*
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STAT3 Transcription Factor / metabolism
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Tamoxifen / pharmacology
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Tumor Suppressor Protein p53 / genetics
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Tumor Suppressor Protein p53 / metabolism
Substances
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3' Untranslated Regions
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Antineoplastic Agents, Phytogenic
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Estrogen Antagonists
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MIRN17 microRNA, human
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MicroRNAs
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STAT3 Transcription Factor
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Tumor Suppressor Protein p53
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Tamoxifen
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Paclitaxel